Smoking as a cofactor for causation of chronic pancreatitis: a meta-analysis.

Pier Luigi Almasio, Angelo Andriulli, Patrick Maisonneuve, Generoso Uomo, Italo Vantini, Edoardo Botteri

Risultato della ricerca: Article

74 Citazioni (Scopus)

Abstract

OBJECTIVES: To assess the evidence for tobacco smoking as a risk factor for the causation of chronic pancreatitis. METHODS: We performed a meta-analysis with random-effects models to estimate pooled relative risks (RRs) of chronic pancreatitis for current, former, and ever smokers, in comparison to never smokers. We also performed dose-response, heterogeneity, publication bias, and sensitivity analyses. RESULTS: Ten case-control studies and 2 cohort studies that evaluated, overall, 1705 patients with chronic pancreatitis satisfied the inclusion criteria. When contrasted to never smokers, the pooled risk estimates for current smokers was 2.8 (95% confidence interval [CI], 1.8-4.2) overall and 2.5 (95% CI, 1.3-4.6) when data were adjusted for alcohol consumption. A dose-response effect of tobacco use on the risk was ascertained: the RR for subjects smoking less than 1 pack per day was 2.4 (95% CI, 0.9-6.6) and increased to 3.3 (95% CI, 1.4-7.9) in those smoking 1 or more packs per day. The risk diminished significantly after smoking cessation, as the RR estimate for former smokers dropped to a value of 1.4 (95% CI, 1.1-1.9). CONCLUSIONS: Tobacco smoking may enhance the risk of developing chronic pancreatitis. Recommendation for smoking cessation, besides alcohol abstinence, should be incorporated in the management of patients with chronic pancreatitis.
Lingua originaleEnglish
pagine (da-a)-
Numero di pagine6
RivistaPancreas
Volume39
Stato di pubblicazionePublished - 2010

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Chronic Pancreatitis
Causality
Meta-Analysis
Smoking
Confidence Intervals
Smoking Cessation
Alcohol Abstinence
Publication Bias
Tobacco Use
Alcohol Drinking
Case-Control Studies
Cohort Studies

All Science Journal Classification (ASJC) codes

  • Hepatology
  • Endocrinology, Diabetes and Metabolism
  • Endocrinology
  • Internal Medicine

Cita questo

Almasio, P. L., Andriulli, A., Maisonneuve, P., Uomo, G., Vantini, I., & Botteri, E. (2010). Smoking as a cofactor for causation of chronic pancreatitis: a meta-analysis. Pancreas, 39, -.

Smoking as a cofactor for causation of chronic pancreatitis: a meta-analysis. / Almasio, Pier Luigi; Andriulli, Angelo; Maisonneuve, Patrick; Uomo, Generoso; Vantini, Italo; Botteri, Edoardo.

In: Pancreas, Vol. 39, 2010, pag. -.

Risultato della ricerca: Article

Almasio, PL, Andriulli, A, Maisonneuve, P, Uomo, G, Vantini, I & Botteri, E 2010, 'Smoking as a cofactor for causation of chronic pancreatitis: a meta-analysis.', Pancreas, vol. 39, pagg. -.
Almasio PL, Andriulli A, Maisonneuve P, Uomo G, Vantini I, Botteri E. Smoking as a cofactor for causation of chronic pancreatitis: a meta-analysis. Pancreas. 2010;39:-.
Almasio, Pier Luigi ; Andriulli, Angelo ; Maisonneuve, Patrick ; Uomo, Generoso ; Vantini, Italo ; Botteri, Edoardo. / Smoking as a cofactor for causation of chronic pancreatitis: a meta-analysis. In: Pancreas. 2010 ; Vol. 39. pagg. -.
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abstract = "OBJECTIVES: To assess the evidence for tobacco smoking as a risk factor for the causation of chronic pancreatitis. METHODS: We performed a meta-analysis with random-effects models to estimate pooled relative risks (RRs) of chronic pancreatitis for current, former, and ever smokers, in comparison to never smokers. We also performed dose-response, heterogeneity, publication bias, and sensitivity analyses. RESULTS: Ten case-control studies and 2 cohort studies that evaluated, overall, 1705 patients with chronic pancreatitis satisfied the inclusion criteria. When contrasted to never smokers, the pooled risk estimates for current smokers was 2.8 (95{\%} confidence interval [CI], 1.8-4.2) overall and 2.5 (95{\%} CI, 1.3-4.6) when data were adjusted for alcohol consumption. A dose-response effect of tobacco use on the risk was ascertained: the RR for subjects smoking less than 1 pack per day was 2.4 (95{\%} CI, 0.9-6.6) and increased to 3.3 (95{\%} CI, 1.4-7.9) in those smoking 1 or more packs per day. The risk diminished significantly after smoking cessation, as the RR estimate for former smokers dropped to a value of 1.4 (95{\%} CI, 1.1-1.9). CONCLUSIONS: Tobacco smoking may enhance the risk of developing chronic pancreatitis. Recommendation for smoking cessation, besides alcohol abstinence, should be incorporated in the management of patients with chronic pancreatitis.",
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T1 - Smoking as a cofactor for causation of chronic pancreatitis: a meta-analysis.

AU - Almasio, Pier Luigi

AU - Andriulli, Angelo

AU - Maisonneuve, Patrick

AU - Uomo, Generoso

AU - Vantini, Italo

AU - Botteri, Edoardo

PY - 2010

Y1 - 2010

N2 - OBJECTIVES: To assess the evidence for tobacco smoking as a risk factor for the causation of chronic pancreatitis. METHODS: We performed a meta-analysis with random-effects models to estimate pooled relative risks (RRs) of chronic pancreatitis for current, former, and ever smokers, in comparison to never smokers. We also performed dose-response, heterogeneity, publication bias, and sensitivity analyses. RESULTS: Ten case-control studies and 2 cohort studies that evaluated, overall, 1705 patients with chronic pancreatitis satisfied the inclusion criteria. When contrasted to never smokers, the pooled risk estimates for current smokers was 2.8 (95% confidence interval [CI], 1.8-4.2) overall and 2.5 (95% CI, 1.3-4.6) when data were adjusted for alcohol consumption. A dose-response effect of tobacco use on the risk was ascertained: the RR for subjects smoking less than 1 pack per day was 2.4 (95% CI, 0.9-6.6) and increased to 3.3 (95% CI, 1.4-7.9) in those smoking 1 or more packs per day. The risk diminished significantly after smoking cessation, as the RR estimate for former smokers dropped to a value of 1.4 (95% CI, 1.1-1.9). CONCLUSIONS: Tobacco smoking may enhance the risk of developing chronic pancreatitis. Recommendation for smoking cessation, besides alcohol abstinence, should be incorporated in the management of patients with chronic pancreatitis.

AB - OBJECTIVES: To assess the evidence for tobacco smoking as a risk factor for the causation of chronic pancreatitis. METHODS: We performed a meta-analysis with random-effects models to estimate pooled relative risks (RRs) of chronic pancreatitis for current, former, and ever smokers, in comparison to never smokers. We also performed dose-response, heterogeneity, publication bias, and sensitivity analyses. RESULTS: Ten case-control studies and 2 cohort studies that evaluated, overall, 1705 patients with chronic pancreatitis satisfied the inclusion criteria. When contrasted to never smokers, the pooled risk estimates for current smokers was 2.8 (95% confidence interval [CI], 1.8-4.2) overall and 2.5 (95% CI, 1.3-4.6) when data were adjusted for alcohol consumption. A dose-response effect of tobacco use on the risk was ascertained: the RR for subjects smoking less than 1 pack per day was 2.4 (95% CI, 0.9-6.6) and increased to 3.3 (95% CI, 1.4-7.9) in those smoking 1 or more packs per day. The risk diminished significantly after smoking cessation, as the RR estimate for former smokers dropped to a value of 1.4 (95% CI, 1.1-1.9). CONCLUSIONS: Tobacco smoking may enhance the risk of developing chronic pancreatitis. Recommendation for smoking cessation, besides alcohol abstinence, should be incorporated in the management of patients with chronic pancreatitis.

UR - http://hdl.handle.net/10447/81124

M3 - Article

VL - 39

SP - -

JO - Pancreas

JF - Pancreas

SN - 0885-3177

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